Dislocation structures inside the cleared dislocation channels in rapid-cooled and tensile-deformed aluminum single crystals were investigated by using transmission electron microscope (TEM). The present study especially focused on the dislocation structures at their early formation stage. In their very beginning stage, arrays of prismatic dislocation loops of the primary slip system were essentially formed elongating along ½ 1 2 1 direction and each prismatic loop stacked to ½ 1 0 1. With the progress of plastic deformation, the number of the prismatic loops composing the array increased and produced tangled structures with dislocations of the primary coplanar slip system. The tangled structures may act as strong obstacles against the following primary dislocations and become a triggering factor for the creation of the cell structure.

-Hyperbaric oxygen (HBO) is a major therapeutic treatment for ischemic ulcerations that perforate skin and underlying muscle in diabetic patients. These lesions do not heal effectively, in part, because of the hypoxic microvascular O 2 partial pressures (PmvO 2 ) resulting from diabetes-induced cardiovascular dysfunction, which alters the dynamic balance between O 2 delivery (Q O2) and utilization (V O2) rates. We tested the hypothesis that HBO in diabetic muscle would exacerbate the hyperoxic Pmv O 2 dynamics due, in part, to a reduction or slowing of the cardiovascular, sympathetic nervous, and respiratory system responses to acute HBO exposure. Adult male Wistar rats were divided randomly into diabetic (DIA: streptozotocin ip) and healthy (control) groups. A small animal hyperbaric chamber was pressurized with oxygen (100% O 2) to 3.0 atmospheres absolute (ATA) at 0.2 ATA/min. Phosphorescence quenching techniques were used to measure Pmv O 2 in tibialis anterior muscle of anesthetized rats during HBO. Lumbar sympathetic nerve activity (LSNA), heart rate (HR), and respiratory rate (RR) were measured electrophysiologically. During the normobaric hyperoxia and HBO, DIA tibialis anterior Pmv O 2 increased faster (mean response time, CONT 78 Ϯ 8, DIA 55 Ϯ 8 s, P Ͻ 0.05) than CONT. Subsequently, Pmv O 2 remained elevated at similar levels in CONT and DIA muscles until normobaric normoxic recovery where the DIA Pmv O 2 retained its hyperoxic level longer than CONT. Sympathetic nervous system and cardiac and respiratory responses to HBO were slower in DIA vs. CONT. Specifically the mean response times for RR (CONT: 6 Ϯ 1 s, DIA: 29 Ϯ 4 s, P Ͻ 0.05), HR (CONT: 16 Ϯ 1 s, DIA: 45 Ϯ 5 s, P Ͻ 0.05), and LSNA (CONT: 140 Ϯ 16 s, DIA: 247 Ϯ 34 s, P Ͻ 0.05) were greater following HBO onset in DIA than CONT. HBO treatment increases tibialis anterior muscle Pmv O 2 more rapidly and for a longer duration in DIA than CONT, but not to a greater level. Whereas respiratory, cardiovascular, and LSNA responses to HBO are profoundly slowed in DIA, only the cardiovascular arm (via HR) may contribute to the muscle vascular incompetence and these faster Pmv O 2 kinetics. (10)-mediated mechanisms, and it is pertinent that chemoreflex (11) and baroreflex control in experimental diabetes is impaired (9, 39). Thus, HBO-induced respiratory, cardiovascular, and baroreflex dysfunction in diabetes can, in addition to altered muscle vascular control, affect the dynamic balance between O 2 delivery (Q O 2 ) and utilization (V O 2 ) [i.e., Pmv O 2 (31, 32)] in skeletal muscle of diabetic patients. An important perspective here is that Pmv O 2 constitutes the sole driving force for blood-tissue O 2 flux, and therefore the beneficial effects of HBO are contingent on Pmv O 2 rising appropriately with HBO. Thus, in understanding the therapeutic potential of HBO, it is important to resolve the time course(s) of Pmv O 2 and these processes (i.e., their kinetics) and gain some insight into their potential to impact tissue Pmv O 2 responses to HBO.Underlyi...

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